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Developmental Effects of Intrauterine and Lactational Exposure to Nanoplastics and Phthalates on Rat Testis
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A new study found that when pregnant rats were exposed to nanoplastics and phthalates (chemicals found in plastics), their male offspring showed lasting damage to testicle development, including changes to sperm-producing cells and increased oxidative stress that persisted into adulthood. The combination of both chemicals caused more harm than either one alone, suggesting that real-world exposure to multiple plastic-related pollutants during pregnancy could pose bigger risks to male reproductive health than scientists previously realized—though more research is needed to confirm these effects translate to humans.
The toxicity of nanoplastics (NPs) and plastic additives such as phthalates, recognized endocrine-disrupting chemicals, remains insufficiently understood, particularly regarding their combined effects on male reproductive health across the lifespan. Since these contaminants can cross biological barriers, including the placenta, this study, grounded in the developmental origins of health and disease (DOHaD) concept, evaluated the effects of gestational and lactational exposure to NPs and a phthalate mixture (PM) on testicular development and function in male offspring. Pregnant SD rats were allocated to six groups: control (CTRL); T1 (20μg/kg/day PM); T2 (200mg/kg/day PM); T3 (NPs: 1mg/kg/day,100nm); T4 (20μg/kg/day PM+NPs); and T5 (200mg/kg/day PM+NPs). Animals were exposed orally from gestational day 10 to postnatal day (PND)21. Male offspring were euthanized at PND22 (prepuberty) and PND120 (adulthood). At PND22, increased apoptosis in pachytene spermatocytes was observed in the T5 group compared with the CTRL, along with altered gene expression, including increased Amh (T4 vs.T1) and Srd5a1 (T1-T4 vs.CTRL) and reduced Ar expression (T3 vs.CTRL). At PND120, the exposure decreased seminiferous tubule diameter (T2), epithelial height (T1-T5), and numbers of Sertoli (T2-T5) and Leydig cells (T4 and T5) compared to the CTRL. Histopathological alterations were more incident in the T1, T3, T4, and T5 compared to the CTRL, and reduced Tjp1 expression in co-exposed animals suggested impairment of the blood-testis barrier. Redox analyses revealed age-dependent worsening of oxidative stress, particularly in co-exposure groups. Overall, gestational co-exposure to phthalates and NPs disrupts testicular morphology, gene regulation, and redox balance, indicating synergistic and persistent reproductive toxicity.
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Gestational and lactational exposure to phthalates and nanoplastics induces inflammation and oxidative imbalance in the prostate of adult rats
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When pregnant rats were exposed to phthalates (chemicals found in plastics) and nanoplastics, their male offspring showed lasting inflammation, oxidative damage, and hormone-related changes in their prostate glands, even as adults. This suggests that plastic exposure during pregnancy and early life could have long-term effects on prostate health in the next generation, raising concerns about how everyday plastic chemicals might impact human development before birth.
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Pregnant rats were given microplastics during pregnancy, and their male offspring had lower birth weights, smaller testicles, reduced testosterone and luteinizing hormone levels, fewer hormone-producing Leydig cells, and changes in sperm, effects that persisted from birth into adulthood.
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This mouse study found that combined exposure to polystyrene nanoplastics and a common plasticizer chemical (DBP) caused worse damage to male reproductive health than either substance alone. The combination significantly reduced sperm quality, lowered antioxidant defenses, and damaged testicular tissue over 60 days. These findings are concerning because people are often exposed to both nanoplastics and plasticizer chemicals at the same time through food packaging and everyday products.
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Researchers exposed pregnant rats to a mixture of phthalates and nanoplastics, both separately and in combination, to study effects on the placenta and fetal development. They found that combined exposure caused more severe damage to placental structure and antioxidant defenses than either contaminant alone. The study suggests that simultaneous exposure to these common plastic-derived pollutants during pregnancy may compound risks to maternal and fetal health.
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A 60-day study in male mice found that polystyrene nanoplastics and the common plasticizer di-n-butyl phthalate (DBP) each impaired sperm quality and testicular structure, but combining the two caused even greater damage — including tubular degeneration, oxidative stress, and structural lesions — than either substance alone. This suggests that real-world simultaneous exposures to nanoplastics and chemical additives they carry could pose compounded reproductive health risks.
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